Hypokalemia

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Hypokalemia

  • General
    • Most clinically affects the muscles/heart
    • K+ is readily absorbed, thus false hypokalemia is possible with large numbers of metabolically active cells
      • In hypokalemia, the kidneys should respond by secreting <20-25 mEq/day
    • Pseudohypokalemia
      • Insulin Excess
      • Epinephrine
  • Main causes:
    • GI losses (Non-Renal) or Urinary losses (Renal) > Intracellular Shifting (insulin or beta-2 agonists (Albuterol), prednisone) > Decreased Intake
    • Meds: Terbutaline, Epinephrine, Piperacillin
    • Hypothermia
    • Alkalemia
    • Hypokalemic Periodic Paralysis
      • 1) Familial, onset <20 y/o
      • 2) Acquired in hyperthyroidism, Asian/Mexican Men
    • A) GI losses
      • Vomiting
      • Diarrhea (most rapid)
        • May see hypokalemia and hypomagnesemia
        • Typically with metabolic acidosis
        • May not normalize with potassium supplementation
        • Worsened by laxatives or enemas
      • Laxative abuse
        • NAGMA or metabolic Alkalosis
      • Gastroenteritis
        • Not refractory to potassium supplements
      • Tube drainage
      • Inability to absorb
    • B) Renal Losses
      • AKD/CKD
      • Hyperaldosteronism (aldosterone promotes excretion)
        • Hypertension and metabolic alkalosis
      • Uremia
      • DKA (Osmotic Diuresis)
      • Bicarb administration
      • Hypomagnesemia
      • Diuretic Abuse (Thiazide or Loop Diuretics)
        • MCly seen with carbonic Anhydrase Inhibitors, loop diuretics, and thiazides
        • Monitor in Athletes, or in 2 weeks after dose increase
      • Bartter Syndrome, Gitelman Syndrome, Liddle Syndrome
      • Hypokalemia + NAGMA
        • RTA Type 1 and 2
    • NSAIDs, Lithium, Foscarnet
    • Acetazolamide, Topiramate, Aminoglycosides, Tenofovir, Valproic Acid, Chemo
    • C) Intracellular Shifting
      • Medication Induced
        • MCly due to insulin, most typically seen after initial administration of insulin in a patient with DKA (give K+ if <3.3 + DKA prior to insulin)
        • Alkalemia: H+ is pushed out of cells to correct alkalemia while K+ is pushed in
        • B2 Activation: activation pushes K+ into cells
      • Total body potassium is normal and potassium replacement may cause rebound hyperkalemia
      • 0.5 mEq/L or more change
    • Refractory Hypokalemia + Alcoholic
      • Hypomagnesemia inhibits PTH release (Hypocalcemia too)
        • (Magnesium <1.6)
      • Decreased intracellular magnesium leads to excess potassium efflux from renal tubular cells into the lumen (renal potassium wasting)
    • May occur after B12 or folate replacement due to increased cell production
  • Symptoms:
    • Mild: fatigue, myalgias, weakness, cramps, constipation
    • Moderate: Ileus
    • Severe: Cramps, Flaccid paralysis with hyporeflexia, hypoventilation
    • Cardiac arrhythmias (ST depression, T wave flattening, U waves, QT prolongation, Ventricular arrhythmias, Arrest)
    • Glucose intolerance
    • Renal impairment (rhabdomyolysis)
  • W/U:
    • Potassium, Calcium, Magnesium, Urine K, Urine and Serum Osm
    • 1) Urine and Serum K and Osmolality
      • No longer recommended
      • TTKG (Transtubular potassium gradient) is calculated with
      • = (Urine K/Serum K)/ (Urine osm/Serum osm)
        • TTKG <2 suggests non-renal source
        • TTKG >4 suggests it is the result of inappropriate renal secretion of K+
    • 2) Urine K+
      • <20 mEq/L: Extrarenal K+ Loss
        • Get ABG
          • Normal
            • Decreased K+ Intake (rare)
            • Laxative Abuse
            • Copious perspiration
          • Metabolic Acidosis
            • GI Tract
            • Diarrhea
            • Villous Adenoma
            • Fistula

      • 20 mEq/L: Renal K+ Loss

        • Get ABG
          • Metabolic Acidosis
            • RTA
            • Carbonic Anhydrases
            • DKA
            • Ureterosigmoidostomy
          • Metabolic Alkalosis (Redistribution)
      • Other) FeK
        • <9.3%, Urine K+ < 13
          • Diarrhea, Transcellular shift, lack of intake

        • 9.3%, Urine K+ ≥13 (81% sensitive, 86% specific for renal wasting)

          • Hypertensive: Aldosterone effect
          • Not
            • Bicarb low: RTA
            • Bicarb not low:
              • Urine Na/Cl >1.6 or chloride <10: Emesis/Piperacillin
              • Urine Na/Cl 1 or chloride >20: Loops/Thiazides or genetic
  • Treatment
    • Targets: 3.5-4.5 in most, >3 in renal failure, >5 in DKA with decent kidneys
    • CI to enteral K+: Severe, profound shock, NPO
    • Mild (3.0-3.5):
    • Moderate (2.5-2.9):
    • Severe (<2.5):
    • Oral > IV Potassium replacement
    • For every 10mEq of KCL given, serum K+ should rise by 0.1mEq/L
      • Give with saline, not dextrose (drives K+ into cells via insulin secretion)
      • KCL for metabolic alkalosis
      • KHCO3 or K citrate/acetate for metabolic acidosis (NAGMA)
    • IV KCL at a max of 20 mEq/hr via a central line if severe or worse
      • Two infusions of 10mEq/hr in two peripherals if no central
    • Treat concurrent hypomagnesemia
    • Cardiac Arrest/VT/VF
      • 20mEq IV over 2-3 minutes
    • Initiate PPI +/- Amiloride

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